Aflatoxin B1 is known to be one of the most potent chemical carcinogens ever found in the human environment. This and other aflatoxins, unfortunately, are common contaminants in agricultural products. Studies on the carcinogenicity of aflatoxins in rats have shown that aflatoxin B1 is more tumorigenic than aflatoxin G1 in liver. The latter compound, however, induces more tumor formation than the former compound in male kidney. Neither aflatoxin B1 nor G1 are carcinogenic in the kidney of female rats. It would be of interest, therefore, to see (1) Are more mutagenic metabolites being converted from aflatoxin B1 than aflatoxin G1 by rats liver homogenates? (2) Are more mutagenic metabolites being converted from aflatoxin G1 than aflatoxin B1 by kidney homogenates of male rats? (3) Are kidney homogenates from female rats failing to convert aflatoxins B1 and G1 to mutagenic metabolites? (4) Does epoxy hydrase affect the presence of mutagenic metabolites? and (5) Is 2,3 epoxide an active form of aflatoxin metabolites? Conidia are treated with aflatoxin B1 or G1, rat liver or kidney homogenates and a NADPH generating system at 37 degrees C for 2 hours. Epoxy hydrase or epoxy hydrase inhibitor might also be added to the treatment solution. At the end the treated conidia are washed. Treated and untreated conidia are assayed for the presence of ad 3 mutants by the direct method.